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Age-dependent acrylamide neurotoxicity in mice: morphology, physiology, and function
M H Ko1, W P Chen, S Y Lin-Shiau
1Department of Anatomy, College of Medicine, National Taiwan University, Taipei, Taiwan.
Experimental Neurology
|August 17, 1999
Summary
Younger mice are more susceptible to acrylamide intoxication, showing earlier and faster onset of peripheral neuropathy. Pathological changes, including axonal swelling, precede visible neurological symptoms in these animals.
Area of Science:
- Neuroscience
- Toxicology
- Pathology
Background:
- Acrylamide intoxication causes peripheral neuropathy, affecting nerve function and leading to weakness and ataxia.
- Previous research suggests distal axonopathy, with pathology in nerve terminals, but earliest changes and age-related susceptibility remain unclear.
Purpose of the Study:
- To investigate the earliest pathological changes in acrylamide intoxication.
- To compare the susceptibility of young (3-week-old) versus older (8-week-old) mice to acrylamide.
Main Methods:
- Mice of different ages were intoxicated with acrylamide (400 ppm) in drinking water.
- Neurological function was assessed using the rota-rod test and observation for weakness and ataxia.
- Pathological changes in motor nerve terminals and neuromuscular junctions were evaluated using histochemistry and immunocytochemistry.
Main Results:
- Acrylamide intoxication progresses through three stages: initial (nerve terminal swelling), early (hindlimb weakness/ataxia), and late (forelimb involvement).
- Younger mice exhibited significantly earlier onset and faster progression of all intoxication stages compared to older mice.
- Initial pathological changes included axonal swelling in motor nerve terminals, preceding observable neurological deficits.
Conclusions:
- Younger mice are demonstrably more susceptible to acrylamide-induced peripheral neuropathy.
- Axonal swelling in nerve terminals represents the earliest pathological alteration in acrylamide intoxication.
- Pathological changes precede the manifestation of clinical neurological symptoms, highlighting the subclinical impact of acrylamide.